title: Adipocytokine profile, cytokine levels and foxp3 expression in multiple sclerosis: a possible link to susceptibility and clinical course of disease.
abstract: BACKGROUND
  Adipocytokines may be involved in multiple sclerosis (MS) as well as other autoimmune and inflammatory-related diseases. This study aims to compare levels of resistin, visfatin and leptin in three subgroups of MS patients with healthy subjects and also to study their relationship with Foxp3 expression and levels of several pro-inflammatory mediators such as interleukine-1 β(IL-1 β),tumor necrosis factor-α (TNF-α) and human sensitive C-reactive protein (hs-CRP).
  
  
  METHODS
  A total of 391 subjects including 200 healthy controls and 191 MS patients were recruited for this case-control study. Circulating adipocytokines and inflammatory mediators were measured using immunoassay methods. Foxp3 gene expression in peripheral blood mononuclear cells (PBMC) was determined by quantitative real-time PCR. Fat tissue mass was evaluated by using dual energy X-ray absorptiometery (DEXA).
  
  
  RESULTS
  A significant difference was observed in levels of inflammatory mediators, adipocytokines, Foxp3 gene expression and adipose tissue mass between MS patients and healthy controls. All adipocytokines were positively correlated with levels of inflammatory mediators and negatively correlated with Foxp3 expression in MS patients. In controls, there were positive correlations between circulating leptin and resistin with TNF-α and IL-1β in subgroup analysis, the highest levels of TNF-α, IL-1β, hs-CRP, resistin and leptin were observed in primary progressive-MS (PP-MS) patients. Also, expression of Foxp3 and levels of visfatin in relapsing remitting-MS(RR-MS) patients were higher compared with the other subgroups.
  
  
  CONCLUSIONS
  Our findings suggest the potential role of adipocytokines in pathogenesis and severity of MS. Notably, the relationship of adipocytokines levels with inflammatory cytokines as well as clinical features of MS could be considerable in translational medicine and biomarker studies.
authors.affiliation: Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Solaleh
authors.initials: S
authors.lastname: Emamgholipour
authors.forename: Seyede Mahdieh
authors.initials: SM
authors.lastname: Eshaghi
authors.forename: Arash
authors.initials: A
authors.lastname: Hossein-nezhad
authors.forename: Khadijeh
authors.initials: K
authors.lastname: Mirzaei
authors.forename: Zhila
authors.initials: Z
authors.lastname: Maghbooli
authors.forename: Mohammad Ali
authors.initials: MA
authors.lastname: Sahraian
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood / Q000235:genetics; D018450:Disease Progression; D004198:Disease Susceptibility; D005260:Female; D051858:Forkhead Transcription Factors / Q000097:blood / Q000235:genetics*; D015870:Gene Expression; D006801:Humans; D053583:Interleukin-1beta / Q000097:blood / Q000235:genetics; D020738:Leptin / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000097:blood* / Q000235:genetics* / Q000473:pathology; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood / Q000235:genetics; D052243:Resistin / Q000097:blood / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
chemical_list: D015415:Biomarkers; D016207:Cytokines; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D053583:Interleukin-1beta; D020738:Leptin; C499624:RETN protein, human; D052243:Resistin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human